Editor's Note: This article is the first in a two-part series on
Neurofeedback in the Treatment of Substance Abuse. This article
presents evidence of the neurological basis, specifically EEG
dysfunction, underlying addiction that makes it such a complicated
condition to treat, and explains how neurofeedback addresses cognitive,
emotional and physical symptoms. The second part of this article will
include a discussion of the efficacy models of neurofeedback and a
review of the research applying neurofeedback to substance abuse
treatment, as well as address the possible mechanisms of its
effectiveness in addiction.

Over the last two decades a new research and clinical
approach--neurofeedback--has shown promise in the treatment of substance
abuse. This article addresses how it works, what makes it so effective,
why it is a potentially important tool in addiction, the
neurophysiological issues it might address, the existing promising
research and, most importantly, that neurofeedback can be a significant
adjunct to the therapeutic and counseling process with addicts.

The
category of disorders associated with substance abuse is the most
common psychiatric set of conditions affecting an estimated 22 million
people in this country (SAMHSA, 2004). Furthermore, the disorder is
accompanied by serious impairments of cognitive, emotional and
behavioral functioning. These conditions and symptoms so significantly
alter a person's brain and its functioning, that we often refer to the
drug as hijacking the brain, making it very difficult to think logically
and appropriately weigh the consequences of the drug related behavior.

Detoxified addicts have been shown to have significant
alterations in brain electroencephalographic (EEG) patterns and children
of addicts also exhibit EEG patterns that are significantly different
than normal (Sokhadze et al., 2008, for review). This indicates that,
not only are we dealing with the neurological consequences of
drug-related behavior, but there appears to be a genetic pattern as
well, that places certain people at greater risk for addictive
behaviors. The complexity of these factors makes the treatment of
addiction one of the most difficult areas of mental, emotional and
physical rehabilitation.

Multiple factors in
addictionTreating addiction is compounded by the many
factors contributing to its onset and maintenance. Furthermore, the
addiction itself masks many other clinical conditions that become more
evident once the drug user becomes abstinent. In fact, it is frequently
other psychiatric problems that lead to drug abuse as the addict
attempts self-medication. It has also been shown that people with
cognitive disabilities are more vulnerable, and more likely to have a
substance abuse disorder (Moore, 1998). These impairments appear to
include attentional issues as well as the hypo-functioning of the
frontal cortex, sometimes referred to as the executive brain, where
decision making takes place (Fowler, et al., 2007).As a result, we
are learning that no one approach has all the answers. Multiple
mechanisms require multiple considerations and approaches. In addition,
addicts are a diverse group, resulting in the need for many tools and
approaches. It appears that programs offering the most diversified array
of treatment modalities are the most effective (Vaccaro & Sideroff,
2008). That is also why, for example, most programs urge the inclusion
of a 12-step program for ongoing support.

But how do you
address the biological and genetic aspects while also addressing the
traumatic and emotional factors, the social cognitive and attentional
factors? How do you deal with the apparent "procedural memory" and
conditioned factors that cause an abstinent addict, on his or her way
home from work, to all of a sudden take an inappropriate turn and end up
at the drug dealer? Neurofeedback appears to be a tool, a training that
has the facility to address many of these factors associated with
addiction.

History of promising treatmentsOver
the years, there have been a number of developments that have been
promising in the treatment of addiction. Each time a new approach is
identified, it is immediately seen as being the long sought after
"silver bullet" that will solve the addiction problem. This occurred
with the development of methadone, and later Levo-Alpha Acetyl Methadol
(LAAM). When I entered the field in 1976, as a post-doctoral fellow of
the National Institute of Drug Abuse, Naltrexone was gaining popularity.
Naltrexone is a long-acting opiate antagonist that blocks the effects
of opiates, such as morphine, heroin and codeine.

It was
around this time that the importance of addiction-related stimuli was
becoming widely recognized (Wikler, 1984). In research examining the
conditioned aspects of addiction, it was found that stimuli associated
with the drug using behavior could serve as conditioned stimuli that
would trigger an unconditioned psychophysiological response that had
similarities to withdrawal and included anxiety, fear and physiological
arousal (e.g. Sideroff & Jarvik, 1980). This conditioned patterning
of response lead to the proposal that relapse liability might be
determined by exposing addicts to these conditioned stimuli and
monitoring their responses (Sideroff, 1980).

Following this
conditioning model, one potential mechanism of Naltrexone treatment
would be the behavioral extinction of some of the conditioned
associations of addiction. In other words, if the addict attempted to
get high while on Naltrexone, the lack of reinforcing effect might
lessen the conditioned effects of drug related stimuli. This, in turn,
might reduce readdiction liability. All that needed to happen was for
the addict to use, without experiencing any effect; a perfectly
reasonable theoretical assumption. So, not only was Naltrexone expected
to be successful in keeping addicts from using, but it also could
address conditioned aspects of addiction.

When I arrived at
UCLA and the Veterans Administration at Brentwood in 1976, I was
surprised to discover that the treatment program to which I had been
awarded a fellowship, was already eliminated--almost before it began.
With the help of the director of the methadone clinic, I started a new
experimental Naltrexone treatment program, drawing recruits from the
VA's methadone maintenance population.

Unfortunately,
Naltrexone did not meet its high expectations. While many methadone
patients expressed interest in using Naltrexone, the long process of
withdrawing from methadone--necessary in order to begin taking the opiate
antagonist--eliminated more than 80 percent of volunteers. Also, as we
enrolled volunteers, we found that 90 percent of the addicts who began
using Naltrexone never used opiates while on the antagonist; and the 10
percent who did use, only used once. It was as if the addict immediately
experienced this "no reward" condition and thus didn't bother to waste
his money. This, in itself, was an interesting finding, as it showed
this population to be able to demonstrate impulse control under certain
circumstances (Sideroff et al., 1978). As a result, we never had the
opportunity to test our theory of extinction.The use of Naltrexone
for opiate addiction has subsequently been viewed as an unworkable
model. Yet, for the small fraction of individuals who were able to detox
and begin taking Naltrexone, it did change their lives.

Typically,
the "Silver Bullet" has been thought of in terms of a drug; something
that could either eliminate craving or eliminate the high of the drug of
abuse. What have become most useful, have been drugs of substitution,
such as buprenorphine, (Johnson, et al., 2000), as we continue to search
for an effective treatment combination that includes psychotherapy.

EEG
and addictionThe EEG is one objective representation of
how the brain is functioning. The EEG is recorded from scalp electrodes,
and is a representation of electrical activity produced by the
collective firing of populations of neurons in the brain, in the
vicinity of the electrode. Figure 1 presents a chart of brain wave
frequencies and the primary functions associated with their production.
It should be pointed out that this is a gross representation and that
more precise differences--beyong the scope of this article - can be found
when you look at specific single frequencies within each range. While
all frequencies and frequency ranges are important and necessary,
problems arise when there is too much or too little of a particular type
of brain wave; there is difficulty shifting in response to changing
needs; or the EEG is to reactive.

For example, in a healthy
functioning brain, if we look at the amount of theta being produced and
we compared it (using 4-8 Hz) with beta frequencies between 13 and 21 Hz
(cycles per second), there is approximately a 2 to 1 ratio. When we
assess the EEGs of people with Attention Deficit Disorder (ADD), we see
ratios that are 3 to 1 and much higher (Lubar, 2003).

These
higher ratios indicate that the brain is producing too much of the slow
waves relative to the beta waves, where the beta waves represent a more
focused and engaged brain. In other words, these brains are
under-activated. On the other hand, if we look at the EEG patterns of
people with anxiety, worry and tension, there is typically too much
activity occurring in the higher frequencies, usually between 24 and 35
Hz. The EEGs of people with substance abuse problems can show both of
these patterns.

It has been demonstrated that the EEGs of
addicts show specific abnormalities when compared to normative data.
Studies of detoxified alcoholics indicate an increase in absolute and
relative power in the higher beta range, along with a decrease in alpha
and delta/theta power (Saletu, et al., 2002). Low voltage fast
desynchronized patterns (high beta) may be interpreted as demonstrating a
hyper arousal of the central nervous system (Saletu-Z et al., 2004);
and Bauer, showed a worse prognosis for the patient group with a more
pronounced frontal hyper-arousal (Bauer, 2001).The fact that these
EEG patterns as well as alcohol dependence itself are highly inheritable
further supports the biological nature of this disease (Gabrielli et
al., 1982; Schuckit & Smith, 1996; Van Beijsterveldt & Van Baal,
2002).

These specific abnormalities show both a worse
prognosis and a predisposition to development of alcoholism.
Individuals with a family history of alcoholism were found to have
reduced relative and absolute alpha power in occipital and frontal
regions and increased relative beta in both regions compared with those
with a negative family history of alcoholism. In another study, these
abnormalities also were associated with risk for alcoholism (Finn &
Justus, 1999).

Dr. Stephen Sideroff, PhD, is a licensed clinical psychologist, consultant and Assistant Professor in the Psychiatry Department at UCLA and one of the Clinical Directors at Moonview Sanctuary. Dr. Sideroff is an internationally recognized expert in (more...)